Journal List > Korean Circ J > v.37(6) > 1016222

Kim: The Open Artery Hypothesis

Abstract

There is considerable clinical and experimental evidence of the benefit of late reperfusion of infarct-related arteries, referred to as the open artery hypothesis, in patients with acute myocardial infarction who presented too late to salvage at-risk ischemic myocardium. In addition to myocardial salvage, reperfusion of the infarct-related artery prevents infarct expansion, reduces development of ventricular remodeling, and decreases ventricular arrhythmia. The Occluded Artery Trial recently answered a major question related to the open artery hypothesis in a high-risk, asymptomatic patient with an occluded infarct artery. In this review, clinical and experimental evidence of the benefit of the open artery hypothesis will be discussed.

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Fig. 1.
Temporary circumflex coronary artery ligation and infarct size in a dog. Reperfusion after 18 and 25 minutes represents a period of reversible ischemia in which infarct transmurality is negligible. After 40 minutes, 3 hours, and 6 hours, however, reperfusion results showed a graded and time-dependent limitation of infarct size. The infarct size limitation following reperfusion after 40 minutes and 3 hours is significant compared with prolonged coronary artery occlusion (24 hours).4)
kcj-37-235f1.tif
Fig. 2.
Bar graph of left ventricular volume as determined by biplane angiography in survivors of first anterior Q wave infarction with paired studies performed at 3 weeks and 1 year after this initial infarction. Patients with a patent left anterior descending coronary artery at the initial catheterization did not demonstrate progressive enlargement over time. In contrast, patients with an occluded vessel supplying their infarcted region showed time-dependent ventricular enlargement; by 1 year (solid bar), these enlargements had increased above their baseline size († p<0.05) and had greater volumes (*p<0.05) than patients with patent vessels.10) LV: left ventricle.
kcj-37-235f2.tif
Fig. 3.
Univariate survival curves for total mortality by infarct artery patency.9)
kcj-37-235f3.tif
Fig. 4.
Photographs of transverse sections of rat left ventricle (LV) subjected to coronary occlusion for 21 days. A: noninfarcted (normal) sham-control rat with normal thickness of the LV wall. B: myocardial infarction without treatment (control), large transmural infarction of the anterior wall showing considerable thinning of the infarct compared with the septal wall and sham-control. The LV cavity was dilated. C: myocardial infarction with 2-(3-benzoyl-phenyl)-propionic acid(ketoprofen) injection. The LV cavity was more dilated than in the control, and the infarct scar is thinner than that of the control (A: hematoxylin-eosin stain, B&C: Masson's trichrome stain).32)
kcj-37-235f4.tif
Fig. 5.
Baseline left ventricular size and subsequent cardiovascular mortality. Baseline end-diastolic and end-systolic areas measured 11 days post-infarction are represented in quartiles. The figure shows that the 3-year cardiovascular mortality rate was greatest in the patients whose left ventricular size was in the upper quartile early post-infarction.34)
kcj-37-235f5.tif
Fig. 6.
Mechanisms of benefit. Early versus late open artery after acute myocardial infarction.3) AMI: acute myocardial infarction, CHF: congestive heart failure, LV: left ventricle.
kcj-37-235f6.tif
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